IL-6 is a cytokine also called B-cell stimulating factor 2 (BSF2) or interferon β2. IL-6 was discovered as a differentiation factor involved in the activation of B-cell lymphocytes (Non-Patent Document 1), and was later revealed to be a multifunctional cytokine that influences the function of various cells (Non-Patent Document 2). It has been reported to induce maturation of T lymphocyte cells (Non-Patent Document 3).
IL-6 transmits its biological activity via two kinds of proteins on the cell. The first is the IL-6 receptor, which is a ligand-binding protein to which IL-6 binds, with a molecular weight of about 80 kDa (Non-Patent Documents 4 and 5). The IL-6 receptor is present in a membrane-bound form that penetrates the cell membrane. It is expressed on the cell membrane, and also as a soluble IL-6 receptor, which mainly consists of the extracellular region of the membrane-bound form.
The other kind of protein is the membrane protein gp130, which has a molecular weight of about 130 kDa and is involved in non-ligand binding signal transduction. The biological activity of IL-6 is transmitted into the cell through formulation of an IL-6/IL-6 receptor complex by IL-6 and 11-6 receptor followed by binding of the complex with gp130 (Non-Patent Document 6).
Even today, many pancreatic cancer cases are diagnosed at the advanced and unresectable stage. Furthermore, even in cases that have undergone resection, which is the only way a cure can be expected, pancreatic cancer often recurs early after surgery. Meanwhile, chemotherapy is indicated for unresectable cases with good performance status (PS) and major organ function. However, although chemotherapy is currently a standard therapy, its therapeutic effect is insufficient. For example, even when gemcitabine hydrochloride regarded as the first drug of choice is used, the efficacy rate of palliative effects is 23.8%, the median survival time is 5.7 months, and the one-year survival rate is 18% (foreign phase III clinical trial data). In Japan, 20,000 people are diagnosed as having pancreatic cancer each year, and 22,260 people died of this disease in 2004 (statistics reported by the Ministry of Health, Labour and Welfare), and pancreatic cancer is the fifth cause of cancer death.
Neural invasion is one of the modes of invasion characteristic of pancreatic cancer. The present inventors have revealed that: neural invasion is found in almost 100% of pancreatic cancer cases; it is an important prognostic factor; and it causes functional abnormalities of hepatocytes, and thus is correlated with cachectic symptoms such as anemia, impaired performance status (PS), and undernutrition. Furthermore, neural invasion is thought to be the cause of cancer pain and the like, and there are some reports describing that symptoms were relieved to some extent by irradiating predominant sites of neural invasion, or by excising the nerve upstream of the sites. However, the mechanisms of neural invasion and onset of symptoms caused by neural invasion are poorly understood, and thus there is currently little information on control of neural invasion and symptoms caused by neural invasion. Neural invasion is commonly found regardless of cancer types, and it has been reported as a prognostic factor of prostatic cancer, stomach cancer, and head and neck cancer.
The prior-art documents related to the present invention are shown below.    Non-Patent Document 1: Hirano, T. et al., Nature (1986) 324, 73-76    Non-Patent Document 2: Akira, S. et al., Adv. in Immunology (1993) 54, 1-78    Non-Patent Document 3: Lotz, M. et al., J. Exp. Med. (1988) 167, 1253-1258    Non-Patent Document 4: Taga, T. et al., J. Exp. Med. (1987) 166, 967-981    Non-Patent Document 5: Yamasaki, K. et al., Science (1988) 241, 825-828    Non-Patent Document 6: Taga, T. et al., Cell (1989) 58, 573-581